Extensive research shows that childhood experiences and the social environment do not reliably determine adult sexual orientation. Early theories that linked parenting style, family dynamics, or traumatic events to homosexuality have not held up under rigorous study. Large-scale, well-designed investigations find no consistent pattern of childhood upbringing or social circumstance that predicts whether someone will be gay, lesbian, or bisexual.

Mainstream scientific organizations—such as the American Psychological Association and the World Health Organization—reject simple “nurture-only” explanations for sexual orientation. Contemporary views emphasize a complex interplay of biological, developmental, and environmental influences rather than any single social cause. In short, psychosocial factors alone cannot account for who a person is sexually attracted to.

References:

• American Psychological Association, “Answers to Your Questions For a Better Understanding of Sexual Orientation & Homosexuality” (2008).
• Bailey JL, Vasey PL, Diamond LM, et al., “Sexual Orientation, Controversy, and Science,” Psychological Science in the Public Interest (2016).

Research shows that childhood experiences, parenting, upbringing, or social environment do not reliably determine adult sexual orientation. Large-scale, well-designed studies find no consistent link between specific early-life events (such as parenting style, family structure, trauma, or peer influences) and whether a person grows up gay, lesbian, or bisexual. Attempts to explain homosexuality solely by nurture—i.e., by psychosocial or environmental causes—are therefore considered inadequate.

Mainstream scientific positions reflect this evidence. Leading professional bodies (e.g., the American Psychological Association, World Health Organization) state that sexual orientation likely arises from a complex interplay of biological, genetic, hormonal, and environmental factors, and reject simplistic “nurture-only” accounts. In short: childhood experience and social environment may shape many aspects of personality and behavior, but they do not reliably predict or cause adult sexual orientation.

References: American Psychological Association (2011) “Report of the APA Task Force on Appropriate Therapeutic Responses to Sexual Orientation”; World Health Organization materials on sexual orientation and health.

Family and twin studies indicate that genetics contribute to same-sex sexual attraction: relatives of gay people are more likely than average to be gay, and identical twins show higher concordance than fraternal twins. Large-scale genome-wide association studies (GWAS) have not found a single “gay gene.” Instead they identify many common genetic variants, each with very small effects, that together account for a modest portion of variation in same-sex sexual behavior. In other words, genetics is one component among many (including environment and development), and the genetic architecture is polygenic and complex (see Sanders et al. 2017; Ganna et al. 2019).

References: Sanders et al., 2017; Ganna et al., 2019 (GWAS of same-sex sexual behavior).

Family and twin studies indicate that sexual orientation has a heritable component: relatives of gay people are more likely than average to be gay, and identical twins show higher concordance for same-sex attraction than fraternal twins. Large-scale genome-wide association studies (GWAS) have searched for genetic variants linked to same-sex sexual behavior and find many common variants each exerting a very small effect rather than one determinative “gay gene.” This means genetics contributes modestly and polygenically to sexual orientation, interacting with environmental and developmental factors. Key references: Sanders et al., 2017; Ganna et al., 2019 (Science).

Prenatal biological factors refer to influences on sexual development that occur before birth. Three main hypotheses in this area are:

• Hormonal exposures in the womb: Variations in fetal sex hormones (especially androgens) during critical periods of brain development are proposed to shape later sexual attractions. For example, lower fetal androgen action is sometimes linked to greater likelihood of same-sex attraction in males, though findings are complex and not uniform.

• Epigenetic markers: Chemical tags on DNA (epigenetic marks) can modulate gene expression without changing the DNA sequence. Some researchers suggest that epigenetic differences established prenatally could influence brain development and later sexual orientation.

• Maternal immune responses: The “fraternal birth order” effect — where each older biological brother increases the chance a later-born son is gay — has led to a maternal immune hypothesis: maternal antibodies formed in response to male fetal proteins might affect development of subsequent male fetuses’ sexual differentiation.

Overall evidence: Empirical findings support that prenatal biological factors plausibly contribute to sexual orientation, but they are not determinative. Sexual orientation appears to be shaped by multiple interacting biological, developmental, and possibly environmental influences; no single prenatal factor explains all variation (see Bogaert 2018; Bogaert & Skorska 2011).

Selected references:

• Bogaert, A. F. (2018). Biological versus nonbiological explanations of male sexual orientation. Archives of Sexual Behavior, 47(3), 557–570.
• Bogaert, A. F., & Skorska, M. N. (2011). The fraternal birth-order effect: Evidence and mechanisms. In Handbook of the Sociology of Sexualities (pp. 97–112).

Some studies report correlations between sexual orientation and brain structure or function — for example, differences in hypothalamic nuclei, patterns of brain activation, or white-matter organization have been observed in groups of gay and heterosexual people (see Swaab & García-Falgueras 2009). These findings suggest that neurodevelopmental processes (including prenatal hormones, genetics, and early brain maturation) may influence sexual orientation. However, two important caveats apply: (1) correlation does not prove causation — observed brain differences might result from life experiences, identity development, or plasticity rather than cause them; and (2) the reported differences are not specific or consistent enough to predict an individual’s orientation reliably. In short, neurodevelopmental factors plausibly contribute to sexual orientation, but the evidence is complex and does not establish a simple causal pathway.

Reference: Swaab, D. F., & García-Falgueras, A. (2009). Sexual differentiation of the human brain in relation to gender identity and sexual orientation. Frontiers in Neuroendocrinology, 30(3), 275–292.

Most researchers understand sexual orientation as the result of multiple interacting factors rather than a single cause or a conscious choice. “Multifactorial” means genetic influences, prenatal biological conditions (hormonal environment, maternal immune response), brain development, and early-life experiences all contribute. “Probabilistic” means these factors change the likelihood of developing a particular orientation but do not determine it with certainty; different combinations and degrees of influence yield diverse outcomes across individuals.

This view is supported by evidence from twin and family studies (showing heritability but not strict genetic determinism), prenatal hormone and neuroanatomical research, and longitudinal and population studies that find no credible evidence sexual orientation is chosen. The multifactorial, probabilistic model explains why sexual orientation is stable for many people yet varies across individuals and cultures, and why simple causal claims (e.g., “caused solely by genes” or “caused by upbringing”) are inconsistent with the evidence.

References: Savin-Williams, R. C., & Vrangalova, Z. (2013). Mostly heterosexual as a distinct sexual orientation group: A review of the empirical evidence. Review of General Psychology; Bailey, J. M., Dunne, M. P., & Martin, N. G. (2000). Genetic and environmental influences on sexual orientation. Behavior Genetics.

Explanation: Researchers propose that biological events before birth can influence later sexual orientation. Key hypotheses include:

• Hormonal exposures: Variations in fetal androgen (male sex hormone) levels during critical periods of brain development may affect sexual attraction patterns. For example, lower prenatal androgens are often hypothesized to be associated with same-sex attraction in natal males, while higher prenatal androgens are considered in some explanations for same-sex attraction in natal females.

• Epigenetic markers: Chemical modifications to DNA or its associated proteins that regulate gene expression (epigenetic changes) arising during fetal development may alter how genes involved in brain and sexual differentiation are expressed, potentially shaping sexual orientation without changing the genetic code itself.

• Maternal immune responses: The maternal immune hypothesis suggests that maternal antibodies produced in response to male fetuses might, after multiple male pregnancies, influence brain development in later male fetuses in ways linked to increased likelihood of homosexual orientation (a proposed explanation primarily for older-brother effects in men).

Evidence status: Empirical findings provide support for some associations consistent with these ideas (e.g., hormone measures, epigenetic patterns in small samples, and the older-brother effect), but results are mixed and effect sizes are often small. No single prenatal biological factor has been shown to deterministically cause homosexuality; current evidence is suggestive but not conclusive, indicating a likely interplay of multiple biological and environmental influences.

References:

• Bogaert, A. F. (2018). Commentary on prenatal influences on sexual orientation. [See reviews and empirical studies cited therein.]
• Bogaert, A. F., & Skorska, M. N. (2011). The maternal immune hypothesis and older-brother effect literature.

(References summarized for concision; consult the cited authors’ review articles and empirical papers for detailed evidence and methodology.)

Most scientists and scholars agree that sexual orientation—whether someone is gay, lesbian, bisexual, or heterosexual—does not arise from a single cause or from conscious choice. Instead, it is best understood as the outcome of multiple, interacting factors that increase the probability of a given orientation without deterministically fixing it.

Key points:

• Biological influences: Genetic variants, prenatal hormone exposures, and early brain development appear to contribute in ways that modestly raise or lower the likelihood of particular orientations (e.g., twin and genome-wide studies; research on prenatal androgen effects) (See Bailey et al., 2016; Bogaert, 2018).
• Environmental and developmental factors: Non-social biological events (such as prenatal conditions) and early developmental environments can shape sexual attractions. Social experiences and cultural context may influence how people understand and express their attractions, though they do not “cause” orientation in a simple, direct way (Hamer, 1999; Savin-Williams, 2005).
• Probabilistic, not deterministic: These influences interact such that certain combinations make a particular orientation more probable, but none act as an absolute determinant. People with similar genetic or prenatal profiles can develop different orientations.
• Not a choice: Because sexual orientation arises from complex biopsychosocial processes outside conscious control, it is not something a person freely chooses.

References for further reading:

• Bailey, J. M., Hill, K. A., & Martin, N. G. (2016). Genetics of sexual orientation. Annual Review of Genetics.
• Bogaert, A. F. (2018). Biological versus nonbiological influences on sexual orientation: Evidence from multiple lines of research. Archives of Sexual Behavior.
• Savin-Williams, R. C. (2005). The new gay teenager. Harvard University Press.

This multifactorial, probabilistic view aligns with major scientific reviews and explains both population-level patterns and individual variation.